Hydrogen-Rich Saline Inhibits Lipopolysaccharide-Induced Acute Lung Injury and Endothelial Dysfunction by Regulating Autophagy through mTOR/TFEB Signaling Pathway
Identifieur interne : 000424 ( Pmc/Curation ); précédent : 000423; suivant : 000425Hydrogen-Rich Saline Inhibits Lipopolysaccharide-Induced Acute Lung Injury and Endothelial Dysfunction by Regulating Autophagy through mTOR/TFEB Signaling Pathway
Auteurs : Zhiling Fu [République populaire de Chine] ; Ze Zhang [République populaire de Chine] ; Xiuying Wu [République populaire de Chine] ; Jin Zhang [République populaire de Chine]Source :
- BioMed Research International [ 2314-6133 ] ; 2020.
Abstract
Hydrogen-rich saline (HRS) has strong anti-inflammatory, antioxidative stress, and antiapoptotic properties. The study focused on the protection of HRS on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in rat models and the relationship with autophagic regulation and mTOR/TFEB signaling pathway.
HRS attenuated LPS-induced ALI and apoptosis both in
The results confirmed the protection of HRS in LPS-induced ALI by regulating apoptosis through inhibiting the mTOR/TFEB signaling pathway.
Url:
DOI: 10.1155/2020/9121894
PubMed: 32071922
PubMed Central: 7011387
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Hydrogen-Rich Saline Inhibits Lipopolysaccharide-Induced Acute Lung Injury and Endothelial Dysfunction by Regulating Autophagy through mTOR/TFEB Signaling Pathway</title><author><name sortKey="Fu, Zhiling" sort="Fu, Zhiling" uniqKey="Fu Z" first="Zhiling" last="Fu">Zhiling Fu</name><affiliation wicri:level="1"><nlm:aff id="I1">Department of Anesthesiology, Shengjing Hospital of China Medical University, No. 36 Sanhao Street, Shenyang, Liaoning Province 110004, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Anesthesiology, Shengjing Hospital of China Medical University, No. 36 Sanhao Street, Shenyang, Liaoning Province 110004</wicri:regionArea></affiliation></author><author><name sortKey="Zhang, Ze" sort="Zhang, Ze" uniqKey="Zhang Z" first="Ze" last="Zhang">Ze Zhang</name><affiliation wicri:level="1"><nlm:aff id="I2">Department of Orthopedics, Shenyang 739 Hospital, No. 121 Yellow River North Street, Huanggu District, Shenyang, Liaoning Province 110004, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Orthopedics, Shenyang 739 Hospital, No. 121 Yellow River North Street, Huanggu District, Shenyang, Liaoning Province 110004</wicri:regionArea></affiliation></author><author><name sortKey="Wu, Xiuying" sort="Wu, Xiuying" uniqKey="Wu X" first="Xiuying" last="Wu">Xiuying Wu</name><affiliation wicri:level="1"><nlm:aff id="I1">Department of Anesthesiology, Shengjing Hospital of China Medical University, No. 36 Sanhao Street, Shenyang, Liaoning Province 110004, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Anesthesiology, Shengjing Hospital of China Medical University, No. 36 Sanhao Street, Shenyang, Liaoning Province 110004</wicri:regionArea></affiliation></author><author><name sortKey="Zhang, Jin" sort="Zhang, Jin" uniqKey="Zhang J" first="Jin" last="Zhang">Jin Zhang</name><affiliation wicri:level="1"><nlm:aff id="I1">Department of Anesthesiology, Shengjing Hospital of China Medical University, No. 36 Sanhao Street, Shenyang, Liaoning Province 110004, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Anesthesiology, Shengjing Hospital of China Medical University, No. 36 Sanhao Street, Shenyang, Liaoning Province 110004</wicri:regionArea></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">32071922</idno><idno type="pmc">7011387</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7011387</idno><idno type="RBID">PMC:7011387</idno><idno type="doi">10.1155/2020/9121894</idno><date when="2020">2020</date><idno type="wicri:Area/Pmc/Corpus">000424</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000424</idno><idno type="wicri:Area/Pmc/Curation">000424</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Curation">000424</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Hydrogen-Rich Saline Inhibits Lipopolysaccharide-Induced Acute Lung Injury and Endothelial Dysfunction by Regulating Autophagy through mTOR/TFEB Signaling Pathway</title><author><name sortKey="Fu, Zhiling" sort="Fu, Zhiling" uniqKey="Fu Z" first="Zhiling" last="Fu">Zhiling Fu</name><affiliation wicri:level="1"><nlm:aff id="I1">Department of Anesthesiology, Shengjing Hospital of China Medical University, No. 36 Sanhao Street, Shenyang, Liaoning Province 110004, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Anesthesiology, Shengjing Hospital of China Medical University, No. 36 Sanhao Street, Shenyang, Liaoning Province 110004</wicri:regionArea></affiliation></author><author><name sortKey="Zhang, Ze" sort="Zhang, Ze" uniqKey="Zhang Z" first="Ze" last="Zhang">Ze Zhang</name><affiliation wicri:level="1"><nlm:aff id="I2">Department of Orthopedics, Shenyang 739 Hospital, No. 121 Yellow River North Street, Huanggu District, Shenyang, Liaoning Province 110004, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Orthopedics, Shenyang 739 Hospital, No. 121 Yellow River North Street, Huanggu District, Shenyang, Liaoning Province 110004</wicri:regionArea></affiliation></author><author><name sortKey="Wu, Xiuying" sort="Wu, Xiuying" uniqKey="Wu X" first="Xiuying" last="Wu">Xiuying Wu</name><affiliation wicri:level="1"><nlm:aff id="I1">Department of Anesthesiology, Shengjing Hospital of China Medical University, No. 36 Sanhao Street, Shenyang, Liaoning Province 110004, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Anesthesiology, Shengjing Hospital of China Medical University, No. 36 Sanhao Street, Shenyang, Liaoning Province 110004</wicri:regionArea></affiliation></author><author><name sortKey="Zhang, Jin" sort="Zhang, Jin" uniqKey="Zhang J" first="Jin" last="Zhang">Jin Zhang</name><affiliation wicri:level="1"><nlm:aff id="I1">Department of Anesthesiology, Shengjing Hospital of China Medical University, No. 36 Sanhao Street, Shenyang, Liaoning Province 110004, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Anesthesiology, Shengjing Hospital of China Medical University, No. 36 Sanhao Street, Shenyang, Liaoning Province 110004</wicri:regionArea></affiliation></author></analytic><series><title level="j">BioMed Research International</title><idno type="ISSN">2314-6133</idno><idno type="eISSN">2314-6141</idno><imprint><date when="2020">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><sec><title>Background</title><p> Hydrogen-rich saline (HRS) has strong anti-inflammatory, antioxidative stress, and antiapoptotic properties. The study focused on the protection of HRS on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in rat models and the relationship with autophagic regulation and mTOR/TFEB signaling pathway. <italic>Material and Methods</italic>. The LPS-induced ALI rats' model was established. Pathohistological change in lung tissue was detected by hematoxylin-eosin staining. The inflammatory cytokines were examined by enzyme-linked immunosorbent assay (ELISA). The key apoptosis proteins and autophagy-relevant proteins were analyzed by western blotting. In vitro, HPMEC models of ALI were treated with LPS. The inflammatory cytokines were detected. Apoptosis rate was determined by flow cytometry. The autophagy and mTOR/TFEB signaling pathway-related proteins were detected by western blot and immunohistochemical staining. </p></sec><sec><title>Results</title><p> HRS attenuated LPS-induced ALI and apoptosis both in <italic>vivo</italic> and in <italic>vitro</italic>. HRS attenuated inflammatory response, inhibited apoptosis, induced and activated autophagy in LPS-induced ALI model, and downregulated mTOR/TFEB signaling pathway. The protection of HRS can be blocked by autophagy inhibitor. Moreover, mTOR activator reversed HRS protection and mTOR inhibitor enhanced HRS protection in LPS-induced model and HRS activated autophagy via mTOR/TFEB signaling pathway. </p></sec><sec><title>Conclusion</title><p> The results confirmed the protection of HRS in LPS-induced ALI by regulating apoptosis through inhibiting the mTOR/TFEB signaling pathway.</p></sec></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Perl, M" uniqKey="Perl M">M. Perl</name></author><author><name sortKey="Chung, C S" uniqKey="Chung C">C.-S. Chung</name></author><author><name sortKey="Perl, U" uniqKey="Perl U">U. Perl</name></author><author><name sortKey="Thakkar, R" uniqKey="Thakkar R">R. 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<front><journal-meta><journal-id journal-id-type="nlm-ta">Biomed Res Int</journal-id><journal-id journal-id-type="iso-abbrev">Biomed Res Int</journal-id><journal-id journal-id-type="publisher-id">BMRI</journal-id><journal-title-group><journal-title>BioMed Research International</journal-title></journal-title-group><issn pub-type="ppub">2314-6133</issn><issn pub-type="epub">2314-6141</issn><publisher><publisher-name>Hindawi</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">32071922</article-id><article-id pub-id-type="pmc">7011387</article-id><article-id pub-id-type="doi">10.1155/2020/9121894</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject></subj-group></article-categories><title-group><article-title>Hydrogen-Rich Saline Inhibits Lipopolysaccharide-Induced Acute Lung Injury and Endothelial Dysfunction by Regulating Autophagy through mTOR/TFEB Signaling Pathway</article-title></title-group><contrib-group><contrib contrib-type="author"><contrib-id contrib-id-type="orcid" authenticated="false">https://orcid.org/0000-0003-2052-0938</contrib-id><name><surname>Fu</surname><given-names>Zhiling</given-names></name><xref ref-type="aff" rid="I1"><sup>1</sup></xref></contrib><contrib contrib-type="author"><name><surname>Zhang</surname><given-names>Ze</given-names></name><xref ref-type="aff" rid="I2"><sup>2</sup></xref></contrib><contrib contrib-type="author"><name><surname>Wu</surname><given-names>Xiuying</given-names></name><xref ref-type="aff" rid="I1"><sup>1</sup></xref></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid" authenticated="false">https://orcid.org/0000-0002-2032-8332</contrib-id><name><surname>Zhang</surname><given-names>Jin</given-names></name><email>zhangj_sj@163.com</email><xref ref-type="aff" rid="I1"><sup>1</sup></xref></contrib></contrib-group><aff id="I1"><sup>1</sup>Department of Anesthesiology, Shengjing Hospital of China Medical University, No. 36 Sanhao Street, Shenyang, Liaoning Province 110004, China</aff><aff id="I2"><sup>2</sup>Department of Orthopedics, Shenyang 739 Hospital, No. 121 Yellow River North Street, Huanggu District, Shenyang, Liaoning Province 110004, China</aff><author-notes><fn fn-type="other"><p>Academic Editor: Vasiliki Galani</p></fn></author-notes><pub-date pub-type="collection"><year>2020</year></pub-date><pub-date pub-type="epub"><day>30</day><month>1</month><year>2020</year></pub-date><volume>2020</volume><elocation-id>9121894</elocation-id><history><date date-type="received"><day>23</day><month>9</month><year>2019</year></date><date date-type="rev-recd"><day>19</day><month>12</month><year>2019</year></date><date date-type="accepted"><day>27</day><month>12</month><year>2019</year></date></history><permissions><copyright-statement>Copyright © 2020 Zhiling Fu et al.</copyright-statement><copyright-year>2020</copyright-year><license xlink:href="http://creativecommons.org/licenses/by/4.0/"><license-p>This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</license-p></license></permissions><abstract><sec><title>Background</title><p> Hydrogen-rich saline (HRS) has strong anti-inflammatory, antioxidative stress, and antiapoptotic properties. The study focused on the protection of HRS on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in rat models and the relationship with autophagic regulation and mTOR/TFEB signaling pathway. <italic>Material and Methods</italic>. The LPS-induced ALI rats' model was established. Pathohistological change in lung tissue was detected by hematoxylin-eosin staining. The inflammatory cytokines were examined by enzyme-linked immunosorbent assay (ELISA). The key apoptosis proteins and autophagy-relevant proteins were analyzed by western blotting. In vitro, HPMEC models of ALI were treated with LPS. The inflammatory cytokines were detected. Apoptosis rate was determined by flow cytometry. The autophagy and mTOR/TFEB signaling pathway-related proteins were detected by western blot and immunohistochemical staining. </p></sec><sec><title>Results</title><p> HRS attenuated LPS-induced ALI and apoptosis both in <italic>vivo</italic> and in <italic>vitro</italic>. HRS attenuated inflammatory response, inhibited apoptosis, induced and activated autophagy in LPS-induced ALI model, and downregulated mTOR/TFEB signaling pathway. The protection of HRS can be blocked by autophagy inhibitor. Moreover, mTOR activator reversed HRS protection and mTOR inhibitor enhanced HRS protection in LPS-induced model and HRS activated autophagy via mTOR/TFEB signaling pathway. </p></sec><sec><title>Conclusion</title><p> The results confirmed the protection of HRS in LPS-induced ALI by regulating apoptosis through inhibiting the mTOR/TFEB signaling pathway.</p></sec></abstract><funding-group><award-group><funding-source>Shenyang Science and Technology Plan Project of Liaoning Province</funding-source><award-id>F14-231-1–60</award-id></award-group><award-group><funding-source>345 Talent Project</funding-source></award-group></funding-group></article-meta></front><floats-group><fig id="fig1" orientation="portrait" position="float"><label>Figure 1</label><caption><p>HRS attenuated LPS-induced ALI in rat models. (a) Hematoxylin-eosin staining (Scale bar = 50 <italic>μ</italic>m). (b) ELISA assay was used to detected inflammatory factor levels; the number of objects analyzed of rats in rats group is 10. Data were expressed as mean ± SD. Statistically significant differences: <sup><italic>∗</italic></sup>indicates <italic>P</italic> < 0.05. ALI: acute lung injury; HRS: Hydrogen-rich saline. All data were analyzed by one‐way analysis of variance (ANOVA) with Tukey's multiple comparison post hoc test.</p></caption><graphic xlink:href="BMRI2020-9121894.001"></graphic></fig><fig id="fig2" orientation="portrait" position="float"><label>Figure 2</label><caption><p>HRS attenuated ALI-induced apoptosis in rat models. Western blot assay and qRT-PCR were used to observe apoptosis-related protein and gene expression. (a) Western blot assay; (b) qRT-PCR assay; the number of objects analyzed of rats in rats group is 10. Data were expressed as mean ± SD. Statistically significant differences: <sup><italic>∗</italic></sup>indicates <italic>P</italic> < 0.05 ALI: acute lung injury; HRS: Hydrogen-rich saline. All data were analyzed by one‐way analysis of variance (ANOVA) with Tukey's multiple comparison post hoc test.</p></caption><graphic xlink:href="BMRI2020-9121894.002"></graphic></fig><fig id="fig3" orientation="portrait" position="float"><label>Figure 3</label><caption><p>HRS attenuated LPS-induced inflammatory response and inhibited apoptosis. (a) Flow cytometry was used to detect the survival rate of HPMECs. (b) ELISA assay was used to detected inflammatory factor levels. (c) Flow cytometry was used to detect the apoptosis rate of HPMECs. All experiments of cells were repeated three times. Data were expressed as mean ± SD. Statistically significant differences: <sup><italic>∗</italic></sup>indicates <italic>P</italic> < 0.05. LPS: lipopolysaccharide; HRS: Hydrogen-rich saline. All data were analyzed by one‐way analysis of variance (ANOVA) with Tukey's multiple comparison post hoc test.</p></caption><graphic xlink:href="BMRI2020-9121894.003"></graphic></fig><fig id="fig4" orientation="portrait" position="float"><label>Figure 4</label><caption><p>HRS activates autophagy in LPS induced ALI and inhibition of autophagy reverses the protective effect of HRS in LPS induced ALI. (a) and (b) Western blotting was used to observe the expression of LC3-II, P62, and Beclin-1 protein. (c) Hematoxylin-eosin staining (Scale bar = 50 <italic>μ</italic>m). (d) ELISA assay was used to detected inflammatory factor levels. (e) Flow cytometry was used to detect the survival rate of HPMECs. (f) Flow cytometry was used to detect the apoptosis rate of HPMECs. All experiments of cells were repeated three times. Data were expressed as mean ± SD. Statistically significant differences: <sup><italic>∗</italic></sup><italic>P</italic> < 0.05. LPS: lipopolysaccharide; HRS: Hydrogen-rich saline. CQ: chloroquine, an autophagy inhibitor; 3MA: 3-methyladenine, an autophagy inhibitor. All data were analyzed by one‐way analysis of variance (ANOVA) with Tukey's multiple comparison post hoc test.</p></caption><graphic xlink:href="BMRI2020-9121894.004"></graphic></fig><fig id="fig5" orientation="portrait" position="float"><label>Figure 5</label><caption><p>HRS activates autophagy via downregulating mTOR/TFEB signaling pathway. (a) Western blot assay was performed to detect the expression levels of p-mTOR and p-S6. (b) Immunohistochemical assay was performed to detect the expression of TFEB protein (Scale bar = 50 <italic>μ</italic>m). The number of objects analyzed of rats in rats group is 10. Data were expressed as mean ± SD. Statistically significant differences: <sup><italic>∗</italic></sup><italic>P</italic> < 0.05. LPS: lipopolysaccharide; HRS: Hydrogen-rich saline. All data were analyzed by <italic>t</italic>-test.</p></caption><graphic xlink:href="BMRI2020-9121894.005"></graphic></fig><fig id="fig6" orientation="portrait" position="float"><label>Figure 6</label><caption><p>mTOR activator reversed HRS protection effect and mTOR Inhibitor enhanced HRS protection effect in LPS-induced injury. (a) Western blot assay was performed to detect the expression levels of p-mTOR, p-S6 LC3-II, P62, and Beclin-1 protein expression levels. (b) Immunohistochemical assay was performed to detect the expression of TFEB protein (Scale bar = 50 <italic>μ</italic>m). (c) ELISA assay was used to detect inflammatory factor levels. (d) Flow cytometry was used to detect the survival rate of HPMECs. (e) Flow cytometry was used to detect the apoptosis rate of HPMECs. All experiments of cells were repeated three times. Data were expressed as mean ± SD. Statistically significant differences: <sup><italic>∗</italic></sup>indicates <italic>P</italic> < 0.05. LPS: lipopolysaccharide; HRS: Hydrogen-rich saline; MHY1485: an mTOR activator; OSI-027: an mTOR inhibitor. All data were analyzed by one‐way analysis of variance (ANOVA) with Tukey's multiple comparison post hoc test.</p></caption><graphic xlink:href="BMRI2020-9121894.006"></graphic></fig><table-wrap id="tab1" orientation="portrait" position="float"><label>Table 1</label><caption><p>qRT-PCR using gene primers.</p></caption><table frame="hsides" rules="groups"><thead><tr><th align="left" rowspan="1" colspan="1">Gene</th><th align="center" rowspan="1" colspan="1">Primer (5′⟶3′)</th></tr></thead><tbody><tr><td align="left" rowspan="2" colspan="1">Bax</td><td align="center" rowspan="1" colspan="1">Forward: GACACTGGACTTCCTCCGG</td></tr><tr><td align="center" rowspan="1" colspan="1">Reverse: GATTGCTGATGTGGATAC</td></tr><tr><td align="left" rowspan="2" colspan="1">Bcl-2</td><td align="center" rowspan="1" colspan="1">Forward: GGCTACGAGTGGGATACT</td></tr><tr><td align="center" rowspan="1" colspan="1">Reverse: ACACGGCTGCCAGGACGT</td></tr><tr><td align="left" rowspan="2" colspan="1">Caspase-3</td><td align="center" rowspan="1" colspan="1">Forward: ACCACTGGATTTTCTGG</td></tr><tr><td align="center" rowspan="1" colspan="1">Reverse: GCCCAAATAGAGGAGGCT</td></tr><tr><td align="left" rowspan="2" colspan="1">GAPDH</td><td align="center" rowspan="1" colspan="1">Forward: GTCATCAACGGGAAACC</td></tr><tr><td align="center" rowspan="1" colspan="1">Reverse: CATGGAGAAGGCTGGGG</td></tr></tbody></table></table-wrap></floats-group></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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